The link is independent of age and the level of parathyroid hormone, according to Nguyen Nguyen, PhD, of the Garvan Institute of Medical Research in Sydney, Australia.

But there may be a "window of opportunity" to intervene, Nguyen reported at the annual meeting of the American Society for Bone and Mineral Research.

Increasing age and parathyroid hormone levels both have positive relationships with the risk of death, and inverse relationships with vitamin D levels, Nguyen noted, and he and his colleagues hypothesized that vitamin D would have an independent association with mortality.

To test the issue, they looked at the long-running Dubbo Osteoporosis Epidemiology Study, which has been following 1,358 women and 858 men in the city of Dubbo, northwest of Sydney, since 1989.

For this analysis, the researchers randomly selected 413 men who were older than 60 in 1989 and looked at their age, weight, height, history of falls and fractures, and lifestyle factors such as smoking and alcohol consumption, over a 14-year period starting in 1996.

Nguyen and colleagues tested blood samples, taken at baseline, for both parathyroid hormone and vitamin D and correlated them with the mortality rate in the cohort over the study period.

They defined a man as deficient in vitamin D if his serum level of 25(OH)D was less than 50 nanomoles per liter. A level of greater than 75 nanomoles per liter was said to be sufficient, while levels in between were defined as insufficient.

All told, 200 of the men died during the follow-up. On average, those who died were significantly older (P<0.0001) and had significantly lower 25(OH)D levels (P=0.0045) although on average 25(OH)D levels were insufficient rather than deficient.

Nguyen said that the prevalence of deficiency among the living participants was 8%, compared with 18% among those who had died, while 42% of both groups had insufficient levels.

Half of the living men had sufficient vitamin D, compared with 40% of those who had died.

Multivariate analysis, adjusting for factors such as age and parathyroid hormone levels, showed that:

For each standard deviation increase in 25(OH)D levels, the risk of death fell by 19% (HR 0.81, 95% CI 0.68 to 0.96).

Compared with those who were deficient in 25(OH)D, those who had insufficient levels had a 36% decrease in the risk of death (HR 0.64, 95% CI 0.43 to 0.93).

Those who had sufficient levels of 25(OH)D had a 39% decrease in the risk of death compared with those who were deficient (HR 0.61, 95% CI 0.41 to 0.91).

Interestingly, Nguyen said, Kaplan-Meier curves showed that the three groups were not markedly different during the first two years after the study started, suggesting that it might be possible to intervene and prevent some deaths.

The difficulty with the study is that the researchers appear to believe that the low vitamin D led to mortality, according to Geoffrey Nicholson, MD, PhD, of the University of Melbourne in Australia, who was not involved in the study.

But, he told MedPage Today, it's possible that the opposite is true, given that much vitamin D comes from sunlight and that men in ill health -- and therefore more likely to die -- might not get outdoors as much as healthier people.

"Did they die because they had low vitamin D or did they have low vitamin D because they were dying?" Nicholson said. "Is it cause or effect? That's the big problem with that sort of study."

He also said most experts, including himself, would put the cutoff for deficiency at 25 nanomoles per liter of serum, rather than the 50 used by Nguyen and colleagues. "I wouldn't agree with that," he said.

Nguyen did not report specific support for the analysis. He had no disclosures.